Glomerulonephritis in some patients can be a relentless disease with edema, hypertension, heart failure and rapidly progressing renal insufficiency. In others, it is an indolent disease which goes on for years without major damage to the kidneys. At present, there is no serologic test which will differentiate patients who will experience a relatively benign illness from those who will develop renal insufficiency and hypertension. The purpose of this research is to see whether accessory or co-existent auto-allergic phenomena may accelerate renal injury in glomerulonephritis. In preliminary studies, we have found that nephritic patients with renal insufficiency have high levels of serum antiglobulin as measured by highly quantitative paired-label technique technique whereas sera from patients with slowly progressive glomerulonephritis have very little if any serum antiglobulin activity. In animal studaes we find that antiglobulins will accelerate glomerular localization of immunoglobulin. Since antibodies to glomerular basement membrane antigens and the glomerular deposition of antigen-antibody complexes have long been implicated as major causes of glomerular injury in glomerulonephritis, it seems probable that if patients with glomerulonephritis become sensitized to gammaglobulin, deposition of immunoglobulin in their kidneys amay be accelerated. We hope to evaluate patients with glomerulonephritis prospectively, to determine whether and when they develop circulating antiglobulins, tg evaluate the effect of these antibodies on renal function and also to discover whether other autoallergic manifestations, includin humoral or cellular immunity to renal of other tissue antigens develop. In parallel, we propose to study animals immunized with heterologous GBM antigens or in which immune complex glomerulonephritis has been induced to see how frequently and to what extent homoral and/or cellular hypersensitivity to autologous immunoglobulin or other tissue antigens accelerates renal injury.